Studies indicate a link between sleep duration and increased risk for cardiovascular diseases (CVD) (Cappuccio et al., 2011). Endothelial dysfunction, possibly caused by impaired nitric oxide (NO) availability, has been suggested as a potential mechanism linking habitual short sleep duration to CVD (Sauvet et al., 2010). Laser Doppler flowmetry (LDF) to assess the skin blood flow (SkBF) response to thermal provocation provides a simple non-invasive method for evaluating endothelial function in humans (Minson, 2010). Using this approach, we examined the impact of acute sleep restriction (SR) on skin microvascular function. It was hypothesised that skin microvascular capacity would be reduced after SR in comparison to normal sleeping. With local ethical approval and written informed consent, 12 young male subjects (mean ± SEM) (20.5 ± 1.5 years) completed two randomized tests: one following three nights with normal sleep consisting of eight hours sleep per night (1436 ± 2 min; CON); the other test followed three nights of SR comprising two, one hour bouts of sleep per night (349 ± 3.0 min). All subjects were healthy, lean, normotensive, and not taking any cardiovascular medication. Energy and fluid provision, and activities of daily living were consistent between tests. On the morning after the third night, following a period of acclimation, cutaneous thermal hyperaemia was assessed on the forearm using an integrating-probe LDF (Periflux 5000). Arterial blood pressures (contralateral arm) and heart rate were monitored at regular intervals throughout the protocol using an oscillometric blood pressure and pulse monitor (Model HEM704C, Omron) Recordings of the laser Doppler signal were made using Perisoft for Windows 9.0 software. Basal SkBF data was recorded for 10 minutes at a standardized skin temeparture of 33°C prior to rapid local heating (1°C min-1) to 42°C, which was maintained for 40 minutes. Location of the LDF probe was the same for both tests. Measurements of SkBF (arbitary perfusion units; APU) were divided by mean arterial pressure (MAP) to give cutaneous vascular conductance (CVC) in APU mmHg-1. Peak plateau (PP) in the SkBF response, which is predominantly dependent on NO, was normalized to baseline (BL) (%CVCBL [((CVC minus CVCBL/CVCBL) x 100]. Following SR; PP was lower at 1182 ± 115 %CVCBL versus CON; 1579 ± 180 %CVCBL (n = 12, P < 0.05, paired t-test). MAPBL was not significantly different; 86 ± 2 versus 86 ± 1 mmHg. This data suggest that in healthy young males acute SR is linked to impaired NO-mediated vasodilator function. Endothelial dysfunction may, in part, explain high CVD morbidity in persons whose sleep is frequently disturbed and insufficient.